Cancer therapy articles within Nature

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  • Editorial |

    Targeted therapies work, but need help to fulfil their potential.

  • News & Views |

    A major hurdle to successful cancer treatment is tumour resistance to chemotherapy. White blood cells called macrophages often infiltrate tumours in large numbers, and now appear to promote tumour chemoresistance.

    • Michele De Palma
    •  & Claire E. Lewis

  • Letter |

    This is one of two papers demonstrating that in several cancer types including ovarian cancer and T-cell leukaemias, the apoptosis regulator MCL1 is targeted for degradation by the FBW7 tumour suppressor. This study finds that this mechanism can determine the response to drugs targeting BCL2 family apoptosis factors. Deletion or mutation of FBW7 found in cancer patients therefore can render tumours resistant to these therapies.

    • Hiroyuki Inuzuka
    • , Shavali Shaik
    •  & Wenyi Wei

  • News & Views |

    The promise of an exciting new drug that inhibits the mutant B-RAF protein in skin cancer is marred by the fact that most patients relapse within a year. Fresh data hint at how such resistance emerges. See Letters p.968 & p.973

    • David Solit
    •  & Charles L. Sawyers

  • News & Views |

    Resistance of tumour cells to chemotherapy can severely affect the efficacy of this anticancer treatment. The non-tumour cells of the organ in which the tumour resides may aid the emergence of such resistance.

    • Urban Emmenegger
    •  & Robert S. Kerbel

  • News |

    Learning how melanoma fights back may yield new therapies.

    • Heidi Ledford

  • News & Views |

    It is hoped that reactivating the tumour-suppressor protein p53 will help to combat cancer. However, fresh evidence suggests it is unlikely that all cells in a tumour will respond to such treatment. See Letters p.567 & p.572

    • Anton Berns

  • Letter |

    p53 is an important tumour suppressor gene. Two papers now show in a Kras-driven lung cancer model that p53-mediated tumour suppression is only engaged late during tumour progression, when the Kras oncogenic signal reaches a threshold sufficient to activate the ARF–p53 pathway. Therefore, p53 re-expression in p53-deficient lung tumours does not restrict early stages of tumorigenesis, but induces tumour regression of more aggressive tumours.

    • David M. Feldser
    • , Kamena K. Kostova
    •  & Tyler Jacks

  • Letter |

    Recent data from early clinical trials in melanoma patients carrying mutations in the B-RAF gene have shown promising results with the B-RAF kinase inhibitor PLX4032; however, many patients eventually develop resistance to this treatment. Two papers now uncover possible mechanisms of resistance to PLX4032. One paper shows that upregulation of MAP3K8 (which encodes COT) can confer resistance of melanoma cells to B-RAF inhibitors, whereas another paper found that melanomas can acquire resistance due to mutations of N-RAS or increased expression of PDGFRβ. Each of these resistance mechanisms seems to apply to at least some patients on recent PLX4032 trial, whereas, surprisingly, so far no secondary B-RAF mutations have been observed.

    • Cory M. Johannessen
    • , Jesse S. Boehm
    •  & Levi A. Garraway

  • Letter |

    Recent data from early clinical trials in melanoma patients carrying mutations in the B-RAF gene have shown promising results with the B-RAF kinase inhibitor PLX4032; however, many patients eventually develop resistance to this treatment. Two papers now uncover possible mechanisms of resistance to PLX4032. One paper shows that upregulation of MAP3K8 (which encodes COT) can confer resistance of melanoma cells to B-RAF inhibitors, whereas another paper found that melanomas can acquire resistance due to mutations of N-RAS or increased expression of PDGFRβ. Each of these resistance mechanisms seems to apply to at least some patients on recent PLX4032 trial, whereas, surprisingly, so far no secondary B-RAF mutations have been observed.

    • Ramin Nazarian
    • , Hubing Shi
    •  & Roger S. Lo

  • News & Views |

    Short residence times in the bloodstream reduce the effectiveness of protein drugs. Application of an approach that combines protein and polymer engineering prolongs circulation time and increases drug uptake by tumours.

    • Jeffrey A. Hubbell

  • News & Views |

    In worms, neurons respond to low levels of environmental oxygen in a way that protects distant tissues from stress-induced cell death. The molecules that mediate this cell-cell signalling may be targets for cancer treatment.

    • Jo Anne Powell-Coffman
    •  & Clark R. Coffman

  • Letter |

    Analogues of migrastatin — a natural product secreted by Streptomyces — are potent inhibitors of tumour cell migration and metastasis. Here, the underlying mechanism is elucidated: these migrastatin analogues target and inhibit the activity of the actin-bundling protein fascin. Hence proteins such as fascin might present new molecular targets for cancer treatments.

    • Lin Chen
    • , Shengyu Yang
    •  & Xin-Yun Huang

  • Letter |

    The four receptors of the Notch family are transmembrane proteins through which mammalian cells communicate to regulate cell fate and growth. Aberrant signalling through each receptor has been linked to disease, so the Notch pathway is a compelling drug target. But current drugs cannot distinguish between the different Notch proteins. Here, phage display technology has been used to generate highly specialized antibodies, enabling the functions of Notch1 and Notch2 to be discriminated in humans and mice.

    • Yan Wu
    • , Carol Cain-Hom
    •  & Christian W. Siebel

  • News & Views |

    Some cancer cells that become tolerant to a drug remain resistant even after its withdrawal, yet these cells eventually become sensitive to the drug again. The underlying molecular mechanism is unusual.

    • Paul Workman
    •  & Jon Travers

  • Letter |

    Cancer 'chemoprevention' uses substances to reverse, suppress or prevent the initial phase of carcinogenesis or the progression of neoplastic cells to cancer cells. Here it is shown that treatment with TRAIL proteins and all-trans-retinyl acetate can cause the death, in vitro and in vivo, of premalignant cells deficient in the adenomatous polyposis coli gene. Normal cells are unaffected. Selectively eliminating premalignant tumour cells in this way is thus an effective method for chemoprevention.

    • Ling Zhang
    • , Xiaoyang Ren
    •  & Xiangwei Wu

  • News & Views |

    Cellular senescence is a physiological mechanism for thwarting the proliferation of tumour cells. Encouraging cancer-prone cells to senesce might therefore be a way to nip this disease in the bud.

    • Manuel Serrano

  • News & Views |

    Inhibitors of RAF enzymes can suppress or activate the same signalling pathway. The details of how this happens provide a cautionary note for those targeting the pathway for anticancer drug discovery.

    • Karen Cichowski
    •  & Pasi A. Jänne

  • News Feature |

    Alan Ashworth took a cancer drug from Petri dish to patients in near record speed. Daniel Cressey meets a biologist who is evangelical about translational research.

    • Daniel Cressey

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